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ESC Congress Reports 2006

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Session Number : 152000
Session Title: Patent foramen ovale Clinical Seminar
Core syllabus topic : Congenital Heart Disease
Prof. Franz Robert Eberli

Prof. Franz Robert Eberli
Date : 3 September 2006

Reported by :
Eberli, F.R.
Zurich, Switzerland

Patent foramen ovale Clinical Seminar

The session was opened by Professor G. Thiene of Padua, Italy, who detailed the anatomy of the patent foramen ovale (PFO). He emphasised that in most instances the PFO is a benign finding and not a pathologic entity. He said that “normally this door is closed and nothing will cross it”. He showed impressive pictures of the large variation of PFOs, ranging in size from 1 to 11 mm in most cases, but up to 20 mm in some cases. He pointed to the gradual transition into a real defect i.e. a small atrial septal defect. Atrial septum aneurysms were the most common additional feature, ranging from a little extra tissue in the septum primum to enormous ballooning of the aneurysmatic septum. Looking at these large aneurysms one could understand the possibility of a thrombus formation within the bulging tissue. He also pointed out the frequent additional abnormality of a large Chiari network in the right atrium. From a functional point of view Professor Thiene stressed that an increase in right atrial pressure is necessary for a paradoxic embolisation to occur.

Dr. Delabay from Morges, Switzerland then focussed on all the possible substances that can cross the PFO in case the door is open, and he outlined the problems and disease states caused by these paradoxically embolised substances: deoxygenated blood, through a massive right to left shunt, might cause systemic hypoxaemia or, if only present in an upright position, a platypnoe-orthodeoxy-syndrome. Air embolism during neurosurgery with the patient in a sitting position might result in a stroke. Gas embolisation might contribute to decompression sickness. In divers suffering a decompression injury a PFO is three times more common than in the normal population (Torti et al. Eur Heart J 2004;25:1014-25). A thrombus might cross the PFO and cause cerebrovascular ischaemia or peripheral emboli. There are several reports depicting this event by echocardiography. However, whether small paradoxic emboli are the cause of most cryptogenic strokes in patients <55 years remains a matter of debate. The likelihood of a paradoxical embolism seems to increase with the size of the PFO. The right to left shunt through the PFO of serotonin, other neurotransmitters or micro emboli might be associated with migraine. Currently, there is an ongoing debate about this relationship. Furthermore, the mechanism by which a PFO could cause migraine remains unclear.

Professor Baudet of Munich followed up on this topic from a neurologist’s point of view. He stressed that migraine is not “just a headache”. It is a neurological, genetically determined disease whose prevalence is 18% in females and 6% in males throughout the universe, independent of ethnic background. Although there is no clear evidence of a cause-effect relationship between migraine and PFO, there is circumstantial evidence of such an association. In migraine patients the prevalence of PFO is 40%, far above the incidence in a normal population. Furthermore, after closure of the PFO for other reasons migraine decreased or disappeared in several trials.

Professor Mullen of London, England then described the technique of percutaneous PFO closure, its expected success rate and complications. He reviewed the data on PFO closure in cryptogenic stroke. He emphasised that although the published studies are all in favour of closing the PFO, there is still no evidence available from randomised trials to help decide whether medical therapy of PFO closure is the preferred method of treatment. However, he pointed out that medical therapy, in particular oral anticoagulation, should not be considered a harmless therapy. He then presented the data of the MIST trial, a double-blind, randomised trial comparing optimal medical therapy to PFO closure in migraine patients. 147 patients with a large PFO and migraine with aura were randomised to receive a STARflex® device for closure of the PFO or no device. Cessation of migraine was achieved in only three of patients with device and was no different to the Sham treated patients. However, migraine decreased by 50% in 42% treated patients vs. 23% of Sham treated patients. These encouraging results will be further explored in several planned clinical trials, the results of which are expected in the next few years.

Many substances (e.g. gas, thrombus, neurotransmitters) can, in the case of increased pressure in the right atrium, cross the PFO. These paradoxical emboli can result in damage in the systemic circulation, such as decompression sickness and cryptogenic stroke. However, the role of paradoxical emboli in all cases of cryptogenic stroke, decompression sickness and, particularly, migraine remains unclear. The ongoing trials comparing closure of the PFO vs. medical therapy might help us not only in deciding about the optimal treatment of these diseases, but also in bringing some insights into the pathophysiology of these diseases.



 
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